Podcast
Questions and Answers
What is a primary consequence of high levels of free radicals in cells?
What is a primary consequence of high levels of free radicals in cells?
- Oxidative stress and cell injury (correct)
- Increased immune function
- Enhanced DNA replication
- Activation of anti-apoptotic proteins
Which type of free radical is classified as a reactive nitrogen species?
Which type of free radical is classified as a reactive nitrogen species?
- Hydroxyl radical
- Superoxide radical
- Hydrogen peroxide
- Nitric oxide (correct)
Which molecule is classified as an endogenous antioxidant enzyme?
Which molecule is classified as an endogenous antioxidant enzyme?
- Peroxiredoxins (correct)
- Glutathione
- Vitamin C
- Vitamin E
What triggers the process of apoptosis?
What triggers the process of apoptosis?
What happens to apoptotic bodies after cell death?
What happens to apoptotic bodies after cell death?
Which of the following diseases is NOT associated with free radical injury?
Which of the following diseases is NOT associated with free radical injury?
Which of the following antioxidants is dietary?
Which of the following antioxidants is dietary?
What is a feature of apoptosis compared to necrosis?
What is a feature of apoptosis compared to necrosis?
What process leads to altered cell metabolism and function in hypoxic injury?
What process leads to altered cell metabolism and function in hypoxic injury?
Which of the following is NOT a consequence of hypoxia on cellular ATP production?
Which of the following is NOT a consequence of hypoxia on cellular ATP production?
What is a potential consequence of reperfusion injury?
What is a potential consequence of reperfusion injury?
What causes free radical formation in the body?
What causes free radical formation in the body?
Which mechanism is directly affected by hypoxia in cells leading to injury?
Which mechanism is directly affected by hypoxia in cells leading to injury?
Which inflammatory mediator is released by white blood cells during reperfusion injury?
Which inflammatory mediator is released by white blood cells during reperfusion injury?
What happens to intracellular calcium levels as a consequence of oxidative stress during reperfusion?
What happens to intracellular calcium levels as a consequence of oxidative stress during reperfusion?
Which condition does NOT contribute to the development of hypoxic injury?
Which condition does NOT contribute to the development of hypoxic injury?
Flashcards are hidden until you start studying
Study Notes
Hypoxic Injury
- Lack of oxygen in tissues leads to altered cell metabolism and function.
- Causes:
- Decreased oxygen content in the blood (hypoxemia).
- Decreased oxygen carrying capacity of blood (anemia).
- Decreased blood flow to the tissue (ischemia).
- Consequences of decreased oxygen delivery to the cell and anaerobic metabolism:
- Decreased ATP production.
- Altered Na+/K+ pump function.
- Altered Ca2+ pump function.
- Decreased protein synthesis.
- Cellular swelling.
- Build-up of lactic acid.
- Release of intracellular enzymes.
- Increased intracellular Ca2+ levels.
Reperfusion Injury
- Cell injury occurring when hypoxic tissue is reperfused after > 60 minutes of hypoxia.
- Factors contributing to reperfusion injury:
- Oxidative stress: Formation of reactive oxygen species (ROS) (i.e., free radicals).
- Ca2+ release: Excess intracellular Ca2+ causes cell injury.
- Inflammation: Release of inflammatory mediators that can cause cell injury (NO, IL-1, TNF, etc), and ROS.
Free Radical Injury
- Free radicals are molecules with an unpaired electron.
- Causes of free radical formation:
- Absorption of extreme energy sources.
- Endogenous, usually oxidative, reactions from normal metabolic processes.
- Inflammation.
- Enzymatic metabolism of exogenous chemicals or drugs.
- Other sources: cigarette smoke, alcohol, pollution, transfats, heavy metals, etc.
- Types of Free Radicals:
- Reactive oxygen species (ROS): Hydroxyl radical (OH-), superoxide radical (O2-), nitric oxide-derived peroxynitrite (ONOO-), hydrogen peroxide (H2O2).
- Reactive nitrogen species (RNS): Nitrogen dioxide (NO2), nitric oxide (NO).
- Effects of Free Radicals:
- Low/moderate levels: Essential for cell metabolism and immune function.
- High levels: Causes 'oxidative stress' and cell injury.
- DNA damage.
- Fragmented proteins.
- Lipid peroxidation.
Clinical Examples of Free Radical Injury
- Free radical injury and aging.
- Free radical injury causes disease:
- Cancer.
- Cardiovascular disease.
- Pulmonary disease.
- Neurodegenerative diseases.
- Ocular disease.
Molecules that Inactivate Free Radicals
- Endogenous antioxidant enzymes: Superoxide dismutase, catalase, peroxiredoxins.
- Non-enzymatic Antioxidants:
- Dietary: Vitamin A, Vitamin C, Vitamin E.
- Glutathione.
Cell Death: Apoptosis
- Programmed cell death.
- Signals that induce apoptosis:
- Extracellular signals: 'death ligands', withdrawal of hormones/growth factors, toxic agents, etc.
- Intracellular signals: Decreased number of anti-apoptotic proteins + production of pro-apoptotic proteins.
- Mechanisms of apoptosis:
- Nucleus condenses and cell shrinks.
- Activation of intracellular enzymes (caspases) that breakdown structural proteins and DNA.
- Apoptotic bodies are ingested by neighboring cells and local phagocytes.
- Note: No activation of the inflammatory response.
Clinical Examples of Apoptosis
- Apoptosis during embryonic development.
- Apoptosis in cancer cells.
Studying That Suits You
Use AI to generate personalized quizzes and flashcards to suit your learning preferences.
